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Role of thyroid hormones in the developmental control of tissue glycogen in fetal sheep near term



Role of thyroid hormones in the developmental control of tissue glycogen in fetal sheep near term



Experimental Physiology 94(10): 1079-1087



Developmental and glucocorticoid-induced changes in tissue glycogen content occur in the fetus near term coincident with an increase in plasma triiodothyronine (T(3)), although the role of thyroid hormones in mediating these changes is unknown. This study investigated glycogen content in the liver, heart and skeletal muscle of sheep fetuses after experimental manipulation of thyroid hormone concentration in utero by T(3) infusion and fetal thyroidectomy (TX). At 130 days of gestation (term 145 +/- 2 days), hepatic glycogen was greater, and muscle glycogen was lower, in the TX fetuses than in the intact fetuses. However, between 130 and 144 days of gestation the normal increment in hepatic glycogen, and decrement in cardiac glycogen, seen in intact fetuses was abolished when the prepartum rise in T(3), but not cortisol, was prevented by TX. At 144 days of gestation, hepatic glycogen was lower, and cardiac glycogen was higher, in the TX compared with intact fetuses. In intact fetuses at 130 days of gestation, 5 days of intravenous T(3) infusion (8-12 microg kg(-1) day(-1)) caused a small but significant increase in hepatic glycogen, although the concentration achieved was not as great as that observed in intact fetuses infused with cortisol (2-3 mg kg(-1) day(-1)) for 5 days. Infusion of T(3) reduced cardiac glycogen to the level observed in mature fetuses near term and immature fetuses infused with cortisol for 5 days. Glycogen content in fetal skeletal muscle increased between 100 and 115 days of gestation, but was unaffected by cortisol or T(3) infusion. Therefore, thyroid hormones are important in the developmental control of hepatic and cardiac glycogen content in the ovine fetus near term and may mediate, in part, the maturational effects of cortisol.

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Accession: 055614859

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PMID: 19542188

DOI: 10.1113/expphysiol.2009.048751


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